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Pathogenesis of dental caries

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Ujwal Gautam
, Dental Intern at B. P. Koirala Institute of Health Sciences, Dharan
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Published on Jul 23, 2012

Pathogenesis of Dental Caries

Published in: Education, Health & Medicine, Business

3 Comments
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Notes

Kieran Ghimire at B.P. Koirala Institute of Health Sciences

been through yyour other works. good job

11 months ago

Ujwal Gautam , Dental Intern at B. P. Koirala Institute of Health Sciences, Dharan

@Shirdent what i meant to mention in my slide was that plaque forms some sort of
scafoldding to localise the acidic content on the tooth surface that ultimately leads to
demineralisation. i only mean to highlight the role of plaque here. However, acidic saliva
can rather be taken as an indicator for the caries susceptibility and i agree with your
opinion that it should be discovered and prophylactic measures be taken. and i appreciate
your kind concern

1 year ago

Shirley Gutkowski , Educator, writer, speaker at Cross Link Presentations

 I disagree with the statement on slide 20. While acidic saliva my not cause decay directly
acidic saliva sets up an environment that will be hospitable to cariogenic, aciduric,
acidophilic bacteria. Acidic saliva should be discovered and treated as contributing to
dental decay, and caries infections.

1 year ago

Pathogenesis of dental caries

1. 1. Pathogenesis ofDental Caries Ujwal Gautam 431, BDS 2009 College of Dental
Surgery, BPKIHS
2. 2. SUGAR + TEETH + MICRO-ORGANISMS ORGANIC ACID Caries Caries
Tetralogy, Newbrun, 1982
3. 3. Dental Caries Dental Caries is an irreversiblemicrobial disease of the calcifiedtissues
of the teeth, characterizedby de-mineralisation of inorganicportion and destruction of
organicsubstance of the tooth, which oftenleads to cavitation.Shafer‘s Textbook of Oral
Pathology, 6th edition
4. 4.  Can remineralisation explain the reversibility? Caries initiation is due to
demineralisation of inorganic component and destruction of organic component. Which
occurs first? Does cavitation necessarily involve in the carious process?
5. 5. Role of Carbohydrates• Carbohydrate caries content in diet incidence suggested by;
HopeWood House Study, Sullivan and Harris- 1958, Harris-1963 Vipeholm Study,
Gustaffson et al, 1954 Patient with Hereditary Fructose Intolerance have less chance of
developing caries, Newbrun- 1969
6. 6. Role of CarbohydratesFermentable Carbohydrates CARIOGENIC BACTERIA acid
7. 7. Role of CarbohydratesCariogenicity of Carbohydrates determined by:Sticky, solid
Carbohydrate more cariogenic than liquidMono or di- saccharides more cariogenic than
poly saccharideIncreased frequency of diet has more chance of cariogenicityIn-between
diets increase the chance of caries Sucrose is more cariogenic than fructose While
Xylitol, sorbitol and Sachharin are found to be non- cariogenic.
8. 8. Role of CarbohydratesCariogenicity of Starch???• Starch are very slowly diffused into
the diet and they also require extra cellular amylase to become hydrolysed before they
can be assimilated and metabolised by plaque bacteria.
9. 9. Role of Carbohydrates• Role of Salivary Carbohydrates??? »NO EFFECT as they are
bound to proteins and are not available for microbial degradation
10. 10. Role of microorganisms Antoni Van Leeuwenhock (1632-1723)indicated the
presence of microorganisms in the scrappings obtained from the carious lesion of tooth
surface Erdl, in 1843, first associated filamentousmicroorganisms to caries on a causative
basis ___ Parasitic Theory
11. 11. Evidence for role of microorganisms: – Oral organisms can demineralise tooth
enamel in vitro and produce lesions similar to the naturally occurring dental caries;
Miller, 1889 – Streptococcus mutans is invariably isolated from carious lesions in the
teeth of British patients; Clark, 1924 – certain bacteria with acidogenic potential can be
isolated and identified from the carious lesions; Florestano, 1942
12. 12. • S. mutans : development of early carious lesions in enamel• Lactobacilli : associated
with dentinal caries• Actinomyces : associated with root surface caries• Vellionella:
possibly anti-cariogenic
13. 13. • Catalase -ve, gram +ve, facultative anaerobic cocci • Grow as convex colonies in
mitis salivarius bacitracin agarCariogenicity due to: • Aciduric, can survive at pH as low
as 4.2 • Present in large number in saliva • Can adhere to acquired pellicle thus
facilitating plaque formation • Can adhere and grow even in hard and smooth tooth
surfaces • Homofermentive; lactic acid being the major productRole of S. mutans: a)
Lactic acid production b) Formation of adhesive plaques c) Production of fermentable
sugars
14. 14. Sucrose glucose + fructose invertase Glucosyl Fructosyl transferase transferase
enzymesproduced by S. mutans glucans fructans Promote reservoir accumulation for of
plaque fermentable sugars for oral bacteria
15. 15. • gram +ve, non spore forming rods • grow best in microaerophilic condition • grows
in rogosa agar (low pH suppresses others) acidogenic + aciduric Possibility as Secondary
invaders due to their acidophilic naturePredominant site of attack are deep fissures and
deep dentinal lesions
16. 16. Role of acid―..dental caries is caused by acid formed by fermentation of food
particles around the teeth‖Robertson, 1835___Chemical (acid) theory
17. 17. Role of acid ―.. dental caries is caused by acid produced by microorganismsfrom the
fermentation of dietary carbohydrates‖ W. D. Miller, 1889 _____ Miller’s
Chemicoparasitic TheoryChemical Theory Parasitic Theory  most accepted & backbone
of current knowledge and understanding of etiology of Dental caries
18. 18. Role of acid ACID CAUSE DISSOLUTION OF THE HYDROXYAPATITE
CRYSTALS OF THE ENAMEL FOLLOWED BY DENTINE (Demineralisation)•
Major degradation product of carbohydrates; Lactic acid Butyric acid Resulting from
anaerobic catabolism
19. 19. Role of acid mere presence of acid is of less significance‗acidic saliva causes tooth
decay‘Localisation of acid upon tooth surface holding mechanism = Dental Plaque
20. 20. Role of Dental Plaque Miller ruled out • Plaque is the soft, non role of Plaque in
mineralised, thin Carious process and transparent film regarded it as a predominently
consisting of protective layer over the enamel micro organisms suspended in salivary
mucins and extracellular bacterial G. V. Black, 1889, associated Dental polysaccharides.
Plaque with caries • Initiation of Plaque is with and described it as formation of acquired
a separate identity pellicle from salivary glycoproteins which later Bibby described the
harbors organisms such as S. nature of plaque, sanguis, A. viscous, A. its role in caries
naeslundii, Veillonellae aka and adherence on pioneering organisms tooth surface • S.
mutans appears in due course
21. 21. Plaque Hypotheses TheoriesNon-Specific Plaque Hypothesis purports thecaries
disease is an outcome of the overallactivity of the total plaque microflora andnot a
specific organism.Specific Plaque Hypothesis proposes that amongthe diverse collection
of bacteriaencompassing the plaque microflora, only a fewspecies of bacteria are
involved in thedisease. The plaque per se is not pathogenic,but the presence of
pathogenic species withinthe plaque causes dental caries.
22. 22.  Harbors the cariogenic bacteria on tooth surface Acid production on plaque-tooth
interface through fermentation of carbohydrates Localisation of acid thus produced
Prevents the diffusion of acid Restrict the buffering action of saliva
23. 23. Buffering capacity of Saliva » Bicarbonate » Urea » Arginine-rich proteins **
Sellman, 1949 found that total amount of acidrequired to reduce the salivary pH is always
greater for saliva from caries resistant persons• Initiation of caries occurs at pH 5.2 - 5.5;
At 5.5 pH, saliva ceases to be saturated with calcium and phosphate leading to the
dissolution of inorganic components of tooth  CRITICAL pH
24. 24. describes the changes in pH ocurring within dental plaquewhen it is subjected to a
carbohydrate diet
25. 25. Homeostasis at normal pHSaliva is supersaturated with respect to enamel Sali
Ca+aPRP va Ca+statherin [Ca] [PO4] [Ca] [PO4] Enamel Ca10(PO4)6OH2
26. 26. DemineralizationDietary CHO + biofilm = lactic acid; diffusion into enamel = local
pH drop Sal [Ca] Ca+aPRP iva Ca+statherin [PO ] 4 [Ca] [PO4] [Ca] [PO4] to exit saliva
CHO + CHO CHO [H ] [H+] [H+] Enamel [H+] Enamel [H+] solubility increases
Ca10(PO4)6OH2
27. 27. pH at enamel‗plaque-tooth interface‘  demineralization less than 5.5 process
beginsloss of calcium and phosphates from the surface and subsurface enamel, creating a
white spot lesion. 1st detectable evidence of Enamel demineralisation frank cavitation if
the bacterial plaque is not regularly removed from the tooth surface.
28. 28. RemineralizationSaliva flow clears CHO; salivary HCO3 returns pH to normal
Sal[Ca] iva 3] statherin Ca+aPRP[PO4] [HCO CHOmove into [Ca] [PO4] [Ca]
[PO4]enamel [HCO3] [HCO3] CHOEnamel Enamelbecomeslesssoluble
Ca10(PO4)6OH2
29. 29. demineralization process is reversible provided that the acidogenic properties of the
biofilm are neutralized. Buffering capacity of salivaIf dietary carbohydrates are removed
/ pH = 7  REMINERALISATION occurs Once the pH returns to higher than the critical
point, demineralization isarrested and minerals can be added back to the partially
dissolved enamel crystallites.
30. 30. Alternating cycles ofDemineralisation & Remineralisation • Net loss – Subsurface
demineralization – New caries – Progression of old lesions • Net gain - remineralization
of existing lesions
31. 31. Remineralization, a conservative alternative to conventional caries removal and
dental restoration• natural process for repairing subsurface non-cavitated carious lesions
caused by organic acids created by bacterial metabolism of fermentable carbohydrates.•
Fluoride ions in the presence of calcium and phosphate promote remineralization by
building a new surface on existing crystal remnants in subsurface demineralized lesions
thus favoring the formation of the more favored fluorapatite crystal in the enamel.
32. 32. Dental cariesRobert H Selwitz, DDS, Amid I Ismail, DrPH and Nigel B Pitts, BDS
The Lancet Volume 369, Issue 9555, Pages 51-59 (January 2007) DOI: 10.1016/S0140-
6736(07)60031-2Diagram of thecaries process asregular flux
ofdemineralisation(destruction) andremineralisation(repair); Adapted fromKidd and
Joyston-Bechal,199749 Copyright © 2007 Elsevier Ltd Terms and Conditions
33. 33. Caries, a Proteolytic processProteolytic enzymes liberated by cariogenic bacteria
destruction of the organic matrix detachment of inorganic crystals from one another
 collapse of whole structure CAVITATION. Gottlieb (1994) and Gottlieb, Diamond and
Applebaum (1946) _______ Proteolytic theory
34. 34. however,• Proteolytic bacteria are rare in oral cavity• No explanation for role of
carbohydrates, acid, etc in dental caries• Carious lesions cannot be reproduced in vitro by
the proteolytic mechanisms• Gnotobiotic studies: caries can occur in absence of
proteolytic organisms.• Enamel is largely inorganic. So, the caries initiation from
proteolytic activity is less likelyTHOUGH ITS ROLE IN CARIES PROGRESSION
CANNOT BE RULED OUT
35. 35. CARIES = acidogenic + proteolytic, a possibility? ______ Manley and Hardwick
(1951)Both type of organisms can be present, eachfunctioning independently.Possible
mechanisms; microorganisms invade enamel lamellae, attack enamel and involve
dentine before clinical evidence of caries. Alteration in enamel prior to invasion by
micro organisms through decalcification
36. 36. Proteolytic Chelation theoryProteolytic breakdown of organic portion of enamel
Proteolytic breakdown products + acquired pellicle + food debris = chelating agent
CHELATION  -vely charged chelating agent releases +vely charged Calcium ions from
enamel/dentine Dissolution of inorganic component of tooth _______ Schatz et al, 1955
37. 37. Factors that influence Dental Caries (Workshop on Dental Caries mechanisms &
Control Techniques, University of Michigan, 1947)Host factors ComponentsA. Tooth 1.
Composition 2. Morphologic characteristics 3. PositionB. Saliva 1. Composition a.
Inorganic b. Organic 2. pH 3. Quantity 4. Viscosity 5. Antibacterial factorsC. Diet 1.
Physical factors a. Quality of Diet 2. Local factors a. Carbohydrate content b. Vitamin
content c. Fluorine contentD. Systemic conditions
38. 38. Histological Changes
39. 39. Pit and Fissure cariesDue to Poor self-cleansing/ developmental faults of tooth Early
lesions appear black/ brown; feel soft and ‗catch‘ Region bordering the lesion appear
opaque bluish white Caries follow the direction of enamel rods and thus form cone
shaped lesion with base at DEJ Undermining occurs through lateral spread at DEJ May
penetrate into dentine through dentinal tubules
40. 40. Smooth surface cariesEarliest change is the appearance of whitechalky spot which is
due to the loss ofinterprismatic substance of enamel Earliest microscopic change involves
accentuation of striae of Retzius and Perikymata Appears as well demarcated faint
opacity or yellow/brown pigmentation with adsorption of exogenous materials by porous
region With progression, forms a cone shaped lesion with base towards the tooth surface
Eventual loss of enamel leads to roughening and superficial decalcification
41. 41. Longitudinal ground sections reveal 4 zones Translucent zone advancing front of
enamel lesion appears structureless after imbibition with quinolone in transmitted light
pore volume 1% compared to 0.1% of sound enamel no evidence of protein loss Dark
zone usually present as a dark brown zone in the transmitted light due to excessive
demineralisation shows birefringence with sound enamel after imbibition with quinolone
in polarised light, so called positive zone contains 2-4% pore volume Body of Lesion
area of greatest demineralisation polarised light shows pore volume of 5% near periphery
and 25% in the centre region appears translucent when examined in quinolone under
transmitted light shows birefringence with sound enamel after imbibition with water
Surface zone partial dimeneralisation of 1- 10% pore volume less than 5% of the spaces
 negative birefringence of surface region with water imbibition positive birefringence of
porous subsurfaceregion
42. 42. Dentinal Caries• Defense reaction of pulpo-dentinal complex – Sclerotic dentine –
Reactionary dentine formation – Sealing of dead tracts• Carious destruction –
Demineralisation – Proteolysis
43. 43. Early dentinal changes: Deposition of fat globules Sclerosis of dentinal tubules
Decalcification of wall of dentinal tubules  Pioneer bacteria Microbial invasion:
Proteolytic, AcidogenicAdvanced Dentinal Changes: Decalcification and confluence of
dentinal tubules Thickening of sheath of Neuman Increase in diameter of Dentinal
tubules with lodging of microorganisms Formation of Liquifaction foci Acidogenic
and proteolytic activity Formation of transverse clefts Caries progression with apex
pulpally and base towards enamel
44. 44. Zones in advancing lesion ofdentinal caries:i. Zone of fatty degeneration of Tomes‘
fibresii.Zone of dentinal sclerosisiii.Zone of decalcification of Dentineiv.Zone of
bacterial invasionv. Zone of decomposed dentine
45. 45. Root Caries• Initiates on mineralised cementum and dentin surfaces which have
greater organic component than enamel tissue• On buccal or lingual surface of tooth•
Dental plaque and microbial invasion important aspect• Decalcification of cementum
follows destruction of remaining matrix
46. 46. Arrested caries• No tendency for further progression• Exclusively in occlusal surface•
Large open cavity in which the superficially softened and decalcified dentine is burnished
to a brown, polished hard surface.
47. 47. ORAL HEALTH CONSEQUENCES• apical periodontitis• periapical abscess•
osteomyelitis of the jaw
48. 48. Pathogenesis of Dental Caries  Fermentation of dietary sugars by Oral micro-
organisms  De-mineralisation  Re-mineralisation  Further demineralisation and
Cavitation  Initiation / Formation of Caries
49. 49. Dental Caries is a multifactorial diseaseHistopathologist  stages of lesion viewed
microscopically.Chemist  interrelationship beetween pH, mineral flux and solubility at
tooth-saliva interfaceMicrobiologist  interaction involving oral bacteria and dental tissue
Current concept of caries etiology impliesinterplay of host, microbial floras, substrate and
time as the principle factors
50. 50. References• Shafer, Hine, Levy; Shafer‘s Textbook of Oral Pathology; 6th Ed.;
Elsevier; 2009• Shobha Tandon; Textbook of Pedodontics; 2nd Ed.; Paras Medical
Publisher• M. W. Roberts, J. T. Wright; The Dyanamic Process of Demineralisation and
Remineralisation; Dimensions of Dental Hygiene. July 2009; 7(7): 16, 18, 20-21• J.D.B.
Featherstone; The Continuum of Dental Caries— Evidence for a Dynamic Disease
Process; Journal of Dental Research; July 2004 Vol.83 no. suppl 1• M. Hurlbutt, B.
Novy, D. Young; Dental Caries: A pH- mediated disease; CDHA Journal – Winter 2010•
Alexander V. Zavgorodniy, Ramin Rohanizadeh, Michael V. Swain, Ultrastructure of
dentine carious lesions, Archives of Oral Biology, Volume 53, Issue 2, February 2008,
Pages 124-132, ISSN 0003-9969, 10.1016/j.archoralbio.2007.08.007.
(http://www.sciencedirect.com/science/article/pii/S00 03996907001999)

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